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(TB) disease in HIV co-infected patients contributes to increased mortality by activating innate and adaptive immune signaling cascades that stimulate HIV-1 replication, leading to an increase in viral load. 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{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T86","span":{"begin":303,"end":340},"obj":"Protein"},{"id":"T87","span":{"begin":342,"end":347},"obj":"Protein"},{"id":"T88","span":{"begin":488,"end":493},"obj":"Protein"},{"id":"T89","span":{"begin":912,"end":917},"obj":"Protein"},{"id":"T90","span":{"begin":919,"end":924},"obj":"Protein"},{"id":"T91","span":{"begin":930,"end":935},"obj":"Protein"},{"id":"T92","span":{"begin":972,"end":977},"obj":"Protein"},{"id":"T93","span":{"begin":1053,"end":1058},"obj":"Protein"},{"id":"T94","span":{"begin":1092,"end":1097},"obj":"Protein"},{"id":"T95","span":{"begin":1259,"end":1264},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"Tuberculosis (TB) disease in HIV co-infected patients contributes to increased mortality by activating innate and adaptive immune signaling cascades that stimulate HIV-1 replication, leading to an increase in viral load. Here, we demonstrate that silencing of the expression of the transcription factor nuclear factor of activated T cells 5 (NFAT5) by RNA interference (RNAi) inhibits Mycobacterium tuberculosis (MTb)-stimulated HIV-1 replication in co-infected macrophages. We show that NFAT5 gene and protein expression are strongly induced by MTb, which is a Toll-like receptor (TLR) ligand, and that an intact NFAT5 binding site in the viral promoter of R5-tropic HIV-1 subtype B and subtype C molecular clones is required for efficent induction of HIV-1 replication by MTb. Furthermore, silencing by RNAi of key components of the TLR pathway in human monocytes, including the downstream signaling molecules MyD88, IRAK1, and TRAF6, significantly inhibits MTb-induced NFAT5 gene expression. Thus, the innate immune response to MTb infection induces NFAT5 gene and protein expression, and NFAT5 plays a crucial role in MTb regulation of HIV-1 replication via a direct interaction with the viral promoter. These findings also demonstrate a general role for NFAT5 in TLR- and MTb-mediated control of gene expression."}

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T412","span":{"begin":342,"end":347},"obj":"http://www.uniprot.org/uniprot/O94916"},{"id":"T413","span":{"begin":488,"end":493},"obj":"http://www.uniprot.org/uniprot/O94916"},{"id":"T414","span":{"begin":614,"end":619},"obj":"http://www.uniprot.org/uniprot/O94916"},{"id":"T415","span":{"begin":972,"end":977},"obj":"http://www.uniprot.org/uniprot/O94916"},{"id":"T416","span":{"begin":1053,"end":1058},"obj":"http://www.uniprot.org/uniprot/O94916"},{"id":"T417","span":{"begin":1092,"end":1097},"obj":"http://www.uniprot.org/uniprot/O94916"},{"id":"T418","span":{"begin":1259,"end":1264},"obj":"http://www.uniprot.org/uniprot/O94916"},{"id":"T419","span":{"begin":912,"end":917},"obj":"http://www.uniprot.org/uniprot/Q99836"},{"id":"T420","span":{"begin":930,"end":935},"obj":"http://www.uniprot.org/uniprot/Q9Y4K3"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"Tuberculosis (TB) disease in HIV co-infected patients contributes to increased mortality by activating innate and adaptive immune signaling cascades that stimulate HIV-1 replication, leading to an increase in viral load. Here, we demonstrate that silencing of the expression of the transcription factor nuclear factor of activated T cells 5 (NFAT5) by RNA interference (RNAi) inhibits Mycobacterium tuberculosis (MTb)-stimulated HIV-1 replication in co-infected macrophages. We show that NFAT5 gene and protein expression are strongly induced by MTb, which is a Toll-like receptor (TLR) ligand, and that an intact NFAT5 binding site in the viral promoter of R5-tropic HIV-1 subtype B and subtype C molecular clones is required for efficent induction of HIV-1 replication by MTb. Furthermore, silencing by RNAi of key components of the TLR pathway in human monocytes, including the downstream signaling molecules MyD88, IRAK1, and TRAF6, significantly inhibits MTb-induced NFAT5 gene expression. Thus, the innate immune response to MTb infection induces NFAT5 gene and protein expression, and NFAT5 plays a crucial role in MTb regulation of HIV-1 replication via a direct interaction with the viral promoter. These findings also demonstrate a general role for NFAT5 in TLR- and MTb-mediated control of gene expression."}

{"project":"GO-BP","denotations":[{"id":"T111","span":{"begin":1005,"end":1027},"obj":"http://purl.obolibrary.org/obo/GO_0002218"},{"id":"T110","span":{"begin":1005,"end":1027},"obj":"http://purl.obolibrary.org/obo/GO_0045088"},{"id":"T109","span":{"begin":1005,"end":1027},"obj":"http://purl.obolibrary.org/obo/GO_0002227"},{"id":"T108","span":{"begin":1005,"end":1027},"obj":"http://purl.obolibrary.org/obo/GO_0045087"},{"id":"T107","span":{"begin":1301,"end":1316},"obj":"http://purl.obolibrary.org/obo/GO_0010467"},{"id":"T106","span":{"begin":978,"end":993},"obj":"http://purl.obolibrary.org/obo/GO_0010467"},{"id":"T105","span":{"begin":805,"end":809},"obj":"http://purl.obolibrary.org/obo/GO_0016246"},{"id":"T104","span":{"begin":370,"end":374},"obj":"http://purl.obolibrary.org/obo/GO_0016246"},{"id":"T103","span":{"begin":352,"end":368},"obj":"http://purl.obolibrary.org/obo/GO_0016246"},{"id":"T102","span":{"begin":130,"end":148},"obj":"http://purl.obolibrary.org/obo/GO_0007165"},{"id":"T101","span":{"begin":892,"end":901},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T100","span":{"begin":130,"end":139},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T99","span":{"begin":282,"end":295},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T97","span":{"begin":1126,"end":1136},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T114","span":{"begin":1012,"end":1027},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T113","span":{"begin":1005,"end":1027},"obj":"http://purl.obolibrary.org/obo/GO_0045824"},{"id":"T112","span":{"begin":1005,"end":1027},"obj":"http://purl.obolibrary.org/obo/GO_0045089"}],"text":"Tuberculosis (TB) disease in HIV co-infected patients contributes to increased mortality by activating innate and adaptive immune signaling cascades that stimulate HIV-1 replication, leading to an increase in viral load. Here, we demonstrate that silencing of the expression of the transcription factor nuclear factor of activated T cells 5 (NFAT5) by RNA interference (RNAi) inhibits Mycobacterium tuberculosis (MTb)-stimulated HIV-1 replication in co-infected macrophages. We show that NFAT5 gene and protein expression are strongly induced by MTb, which is a Toll-like receptor (TLR) ligand, and that an intact NFAT5 binding site in the viral promoter of R5-tropic HIV-1 subtype B and subtype C molecular clones is required for efficent induction of HIV-1 replication by MTb. Furthermore, silencing by RNAi of key components of the TLR pathway in human monocytes, including the downstream signaling molecules MyD88, IRAK1, and TRAF6, significantly inhibits MTb-induced NFAT5 gene expression. Thus, the innate immune response to MTb infection induces NFAT5 gene and protein expression, and NFAT5 plays a crucial role in MTb regulation of HIV-1 replication via a direct interaction with the viral promoter. These findings also demonstrate a general role for NFAT5 in TLR- and MTb-mediated control of gene expression."}

{"project":"GO-MF","denotations":[{"id":"T117","span":{"begin":587,"end":593},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T118","span":{"begin":620,"end":627},"obj":"http://purl.obolibrary.org/obo/GO_0005488"}],"text":"Tuberculosis (TB) disease in HIV co-infected patients contributes to increased mortality by activating innate and adaptive immune signaling cascades that stimulate HIV-1 replication, leading to an increase in viral load. Here, we demonstrate that silencing of the expression of the transcription factor nuclear factor of activated T cells 5 (NFAT5) by RNA interference (RNAi) inhibits Mycobacterium tuberculosis (MTb)-stimulated HIV-1 replication in co-infected macrophages. We show that NFAT5 gene and protein expression are strongly induced by MTb, which is a Toll-like receptor (TLR) ligand, and that an intact NFAT5 binding site in the viral promoter of R5-tropic HIV-1 subtype B and subtype C molecular clones is required for efficent induction of HIV-1 replication by MTb. Furthermore, silencing by RNAi of key components of the TLR pathway in human monocytes, including the downstream signaling molecules MyD88, IRAK1, and TRAF6, significantly inhibits MTb-induced NFAT5 gene expression. Thus, the innate immune response to MTb infection induces NFAT5 gene and protein expression, and NFAT5 plays a crucial role in MTb regulation of HIV-1 replication via a direct interaction with the viral promoter. These findings also demonstrate a general role for NFAT5 in TLR- and MTb-mediated control of gene expression."}

{"project":"GO-CC","denotations":[{"id":"T119","span":{"begin":333,"end":338},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"Tuberculosis (TB) disease in HIV co-infected patients contributes to increased mortality by activating innate and adaptive immune signaling cascades that stimulate HIV-1 replication, leading to an increase in viral load. Here, we demonstrate that silencing of the expression of the transcription factor nuclear factor of activated T cells 5 (NFAT5) by RNA interference (RNAi) inhibits Mycobacterium tuberculosis (MTb)-stimulated HIV-1 replication in co-infected macrophages. We show that NFAT5 gene and protein expression are strongly induced by MTb, which is a Toll-like receptor (TLR) ligand, and that an intact NFAT5 binding site in the viral promoter of R5-tropic HIV-1 subtype B and subtype C molecular clones is required for efficent induction of HIV-1 replication by MTb. Furthermore, silencing by RNAi of key components of the TLR pathway in human monocytes, including the downstream signaling molecules MyD88, IRAK1, and TRAF6, significantly inhibits MTb-induced NFAT5 gene expression. Thus, the innate immune response to MTb infection induces NFAT5 gene and protein expression, and NFAT5 plays a crucial role in MTb regulation of HIV-1 replication via a direct interaction with the viral promoter. These findings also demonstrate a general role for NFAT5 in TLR- and MTb-mediated control of gene expression."}

{"project":"sentences","denotations":[{"id":"T63","span":{"begin":1208,"end":1317},"obj":"Sentence"},{"id":"T62","span":{"begin":995,"end":1207},"obj":"Sentence"},{"id":"T61","span":{"begin":779,"end":994},"obj":"Sentence"},{"id":"T60","span":{"begin":475,"end":778},"obj":"Sentence"},{"id":"T59","span":{"begin":221,"end":474},"obj":"Sentence"},{"id":"T58","span":{"begin":0,"end":220},"obj":"Sentence"},{"id":"T4","span":{"begin":0,"end":220},"obj":"Sentence"},{"id":"T5","span":{"begin":221,"end":474},"obj":"Sentence"},{"id":"T6","span":{"begin":475,"end":778},"obj":"Sentence"},{"id":"T7","span":{"begin":779,"end":994},"obj":"Sentence"},{"id":"T8","span":{"begin":995,"end":1207},"obj":"Sentence"},{"id":"T9","span":{"begin":1208,"end":1317},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Tuberculosis (TB) disease in HIV co-infected patients contributes to increased mortality by activating innate and adaptive immune signaling cascades that stimulate HIV-1 replication, leading to an increase in viral load. Here, we demonstrate that silencing of the expression of the transcription factor nuclear factor of activated T cells 5 (NFAT5) by RNA interference (RNAi) inhibits Mycobacterium tuberculosis (MTb)-stimulated HIV-1 replication in co-infected macrophages. We show that NFAT5 gene and protein expression are strongly induced by MTb, which is a Toll-like receptor (TLR) ligand, and that an intact NFAT5 binding site in the viral promoter of R5-tropic HIV-1 subtype B and subtype C molecular clones is required for efficent induction of HIV-1 replication by MTb. Furthermore, silencing by RNAi of key components of the TLR pathway in human monocytes, including the downstream signaling molecules MyD88, IRAK1, and TRAF6, significantly inhibits MTb-induced NFAT5 gene expression. Thus, the innate immune response to MTb infection induces NFAT5 gene and protein expression, and NFAT5 plays a crucial role in MTb regulation of HIV-1 replication via a direct interaction with the viral promoter. These findings also demonstrate a general role for NFAT5 in TLR- and MTb-mediated control of gene expression."}

{"project":"ICD10","denotations":[{"id":"T116","span":{"begin":399,"end":411},"obj":"http://purl.bioontology.org/ontology/ICD10/A15-A19.9"}],"text":"Tuberculosis (TB) disease in HIV co-infected patients contributes to increased mortality by activating innate and adaptive immune signaling cascades that stimulate HIV-1 replication, leading to an increase in viral load. Here, we demonstrate that silencing of the expression of the transcription factor nuclear factor of activated T cells 5 (NFAT5) by RNA interference (RNAi) inhibits Mycobacterium tuberculosis (MTb)-stimulated HIV-1 replication in co-infected macrophages. We show that NFAT5 gene and protein expression are strongly induced by MTb, which is a Toll-like receptor (TLR) ligand, and that an intact NFAT5 binding site in the viral promoter of R5-tropic HIV-1 subtype B and subtype C molecular clones is required for efficent induction of HIV-1 replication by MTb. Furthermore, silencing by RNAi of key components of the TLR pathway in human monocytes, including the downstream signaling molecules MyD88, IRAK1, and TRAF6, significantly inhibits MTb-induced NFAT5 gene expression. Thus, the innate immune response to MTb infection induces NFAT5 gene and protein expression, and NFAT5 plays a crucial role in MTb regulation of HIV-1 replication via a direct interaction with the viral promoter. These findings also demonstrate a general role for NFAT5 in TLR- and MTb-mediated control of gene expression."}

{"project":"simple1","denotations":[{"id":"T169","span":{"begin":303,"end":340},"obj":"Protein"},{"id":"T170","span":{"begin":342,"end":347},"obj":"Protein"},{"id":"T171","span":{"begin":488,"end":493},"obj":"Protein"},{"id":"T172","span":{"begin":912,"end":917},"obj":"Protein"},{"id":"T173","span":{"begin":919,"end":924},"obj":"Protein"},{"id":"T174","span":{"begin":930,"end":935},"obj":"Protein"},{"id":"T175","span":{"begin":972,"end":977},"obj":"Protein"},{"id":"T176","span":{"begin":1053,"end":1058},"obj":"Protein"},{"id":"T177","span":{"begin":1092,"end":1097},"obj":"Protein"},{"id":"T178","span":{"begin":1259,"end":1264},"obj":"Protein"}],"text":"Tuberculosis (TB) disease in HIV co-infected patients contributes to increased mortality by activating innate and adaptive immune signaling cascades that stimulate HIV-1 replication, leading to an increase in viral load. Here, we demonstrate that silencing of the expression of the transcription factor nuclear factor of activated T cells 5 (NFAT5) by RNA interference (RNAi) inhibits Mycobacterium tuberculosis (MTb)-stimulated HIV-1 replication in co-infected macrophages. We show that NFAT5 gene and protein expression are strongly induced by MTb, which is a Toll-like receptor (TLR) ligand, and that an intact NFAT5 binding site in the viral promoter of R5-tropic HIV-1 subtype B and subtype C molecular clones is required for efficent induction of HIV-1 replication by MTb. Furthermore, silencing by RNAi of key components of the TLR pathway in human monocytes, including the downstream signaling molecules MyD88, IRAK1, and TRAF6, significantly inhibits MTb-induced NFAT5 gene expression. Thus, the innate immune response to MTb infection induces NFAT5 gene and protein expression, and NFAT5 plays a crucial role in MTb regulation of HIV-1 replication via a direct interaction with the viral promoter. These findings also demonstrate a general role for NFAT5 in TLR- and MTb-mediated control of gene expression."}

{"project":"BioNLP16_DUT","denotations":[{"id":"T756","span":{"begin":303,"end":340},"obj":"Protein"},{"id":"T757","span":{"begin":342,"end":347},"obj":"Protein"},{"id":"T758","span":{"begin":488,"end":493},"obj":"Protein"},{"id":"T759","span":{"begin":912,"end":917},"obj":"Protein"},{"id":"T760","span":{"begin":919,"end":924},"obj":"Protein"},{"id":"T761","span":{"begin":930,"end":935},"obj":"Protein"},{"id":"T762","span":{"begin":972,"end":977},"obj":"Protein"},{"id":"T763","span":{"begin":1092,"end":1097},"obj":"Protein"},{"id":"T764","span":{"begin":1053,"end":1058},"obj":"Protein"},{"id":"T765","span":{"begin":1259,"end":1264},"obj":"Protein"},{"id":"T767","span":{"begin":247,"end":256},"obj":"Negative_regulation"},{"id":"T768","span":{"begin":264,"end":274},"obj":"Gene_expression"},{"id":"T769","span":{"begin":535,"end":542},"obj":"Positive_regulation"},{"id":"T770","span":{"begin":511,"end":521},"obj":"Gene_expression"},{"id":"T771","span":{"begin":792,"end":801},"obj":"Negative_regulation"},{"id":"T772","span":{"begin":960,"end":971},"obj":"Positive_regulation"},{"id":"T773","span":{"begin":951,"end":959},"obj":"Negative_regulation"},{"id":"T774","span":{"begin":983,"end":993},"obj":"Gene_expression"},{"id":"T775","span":{"begin":1045,"end":1052},"obj":"Positive_regulation"},{"id":"T776","span":{"begin":1076,"end":1086},"obj":"Gene_expression"},{"id":"T777","span":{"begin":1171,"end":1182},"obj":"Binding"}],"relations":[{"id":"R582","pred":"themeOf","subj":"T757","obj":"T768"},{"id":"R583","pred":"themeOf","subj":"T758","obj":"T769"},{"id":"R584","pred":"themeOf","subj":"T758","obj":"T770"},{"id":"R585","pred":"themeOf","subj":"T759","obj":"T771"},{"id":"R586","pred":"themeOf","subj":"T760","obj":"T771"},{"id":"R587","pred":"themeOf","subj":"T762","obj":"T774"},{"id":"R588","pred":"themeOf","subj":"T763","obj":"T777"},{"id":"R589","pred":"themeOf","subj":"T764","obj":"T775"},{"id":"R590","pred":"themeOf","subj":"T764","obj":"T776"},{"id":"R591","pred":"themeOf","subj":"T768","obj":"T767"},{"id":"R592","pred":"themeOf","subj":"T770","obj":"T769"},{"id":"R593","pred":"themeOf","subj":"T774","obj":"T773"},{"id":"R594","pred":"themeOf","subj":"T774","obj":"T772"},{"id":"R595","pred":"themeOf","subj":"T776","obj":"T775"}],"text":"Tuberculosis (TB) disease in HIV co-infected patients contributes to increased mortality by activating innate and adaptive immune signaling cascades that stimulate HIV-1 replication, leading to an increase in viral load. Here, we demonstrate that silencing of the expression of the transcription factor nuclear factor of activated T cells 5 (NFAT5) by RNA interference (RNAi) inhibits Mycobacterium tuberculosis (MTb)-stimulated HIV-1 replication in co-infected macrophages. We show that NFAT5 gene and protein expression are strongly induced by MTb, which is a Toll-like receptor (TLR) ligand, and that an intact NFAT5 binding site in the viral promoter of R5-tropic HIV-1 subtype B and subtype C molecular clones is required for efficent induction of HIV-1 replication by MTb. Furthermore, silencing by RNAi of key components of the TLR pathway in human monocytes, including the downstream signaling molecules MyD88, IRAK1, and TRAF6, significantly inhibits MTb-induced NFAT5 gene expression. Thus, the innate immune response to MTb infection induces NFAT5 gene and protein expression, and NFAT5 plays a crucial role in MTb regulation of HIV-1 replication via a direct interaction with the viral promoter. These findings also demonstrate a general role for NFAT5 in TLR- and MTb-mediated control of gene expression."}

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Here, we demonstrate that silencing of the expression of the transcription factor nuclear factor of activated T cells 5 (NFAT5) by RNA interference (RNAi) inhibits Mycobacterium tuberculosis (MTb)-stimulated HIV-1 replication in co-infected macrophages. We show that NFAT5 gene and protein expression are strongly induced by MTb, which is a Toll-like receptor (TLR) ligand, and that an intact NFAT5 binding site in the viral promoter of R5-tropic HIV-1 subtype B and subtype C molecular clones is required for efficent induction of HIV-1 replication by MTb. Furthermore, silencing by RNAi of key components of the TLR pathway in human monocytes, including the downstream signaling molecules MyD88, IRAK1, and TRAF6, significantly inhibits MTb-induced NFAT5 gene expression. Thus, the innate immune response to MTb infection induces NFAT5 gene and protein expression, and NFAT5 plays a crucial role in MTb regulation of HIV-1 replication via a direct interaction with the viral promoter. These findings also demonstrate a general role for NFAT5 in TLR- and MTb-mediated control of gene expression."}

{"project":"testone","denotations":[{"id":"T31","span":{"begin":1171,"end":1182},"obj":"Binding"},{"id":"T30","span":{"begin":1076,"end":1086},"obj":"Gene_expression"},{"id":"T29","span":{"begin":1045,"end":1052},"obj":"Positive_regulation"},{"id":"T28","span":{"begin":983,"end":993},"obj":"Gene_expression"},{"id":"T27","span":{"begin":964,"end":971},"obj":"Positive_regulation"},{"id":"T26","span":{"begin":951,"end":959},"obj":"Negative_regulation"},{"id":"T25","span":{"begin":792,"end":801},"obj":"Negative_regulation"},{"id":"T24","span":{"begin":535,"end":542},"obj":"Positive_regulation"},{"id":"T23","span":{"begin":247,"end":256},"obj":"Negative_regulation"},{"id":"T22","span":{"begin":1259,"end":1264},"obj":"Protein"},{"id":"T21","span":{"begin":1092,"end":1097},"obj":"Protein"},{"id":"T20","span":{"begin":1053,"end":1058},"obj":"Protein"},{"id":"T19","span":{"begin":972,"end":977},"obj":"Protein"},{"id":"T18","span":{"begin":930,"end":935},"obj":"Protein"},{"id":"T17","span":{"begin":919,"end":924},"obj":"Protein"},{"id":"T16","span":{"begin":912,"end":917},"obj":"Protein"},{"id":"T15","span":{"begin":488,"end":493},"obj":"Protein"},{"id":"T14","span":{"begin":342,"end":347},"obj":"Protein"},{"id":"T13","span":{"begin":303,"end":340},"obj":"Protein"}],"relations":[{"id":"R3","pred":"causeOf","subj":"T18","obj":"T26"},{"id":"R4","pred":"themeOf","subj":"T19","obj":"T28"},{"id":"R5","pred":"themeOf","subj":"T20","obj":"T30"},{"id":"R6","pred":"themeOf","subj":"T21","obj":"T31"},{"id":"R7","pred":"themeOf","subj":"T21","obj":"T29"},{"id":"R8","pred":"themeOf","subj":"T27","obj":"T26"},{"id":"R9","pred":"themeOf","subj":"T28","obj":"T27"},{"id":"R10","pred":"themeOf","subj":"T30","obj":"T29"},{"id":"R1","pred":"equivalentTo","subj":"T14","obj":"T13"},{"id":"R2","pred":"causeOf","subj":"T17","obj":"T26"}],"text":"Tuberculosis (TB) disease in HIV co-infected patients contributes to increased mortality by activating innate and adaptive immune signaling cascades that stimulate HIV-1 replication, leading to an increase in viral load. Here, we demonstrate that silencing of the expression of the transcription factor nuclear factor of activated T cells 5 (NFAT5) by RNA interference (RNAi) inhibits Mycobacterium tuberculosis (MTb)-stimulated HIV-1 replication in co-infected macrophages. We show that NFAT5 gene and protein expression are strongly induced by MTb, which is a Toll-like receptor (TLR) ligand, and that an intact NFAT5 binding site in the viral promoter of R5-tropic HIV-1 subtype B and subtype C molecular clones is required for efficent induction of HIV-1 replication by MTb. Furthermore, silencing by RNAi of key components of the TLR pathway in human monocytes, including the downstream signaling molecules MyD88, IRAK1, and TRAF6, significantly inhibits MTb-induced NFAT5 gene expression. Thus, the innate immune response to MTb infection induces NFAT5 gene and protein expression, and NFAT5 plays a crucial role in MTb regulation of HIV-1 replication via a direct interaction with the viral promoter. These findings also demonstrate a general role for NFAT5 in TLR- and MTb-mediated control of gene expression."}

{"project":"test3","denotations":[{"id":"T45","span":{"begin":342,"end":347},"obj":"Protein"},{"id":"T44","span":{"begin":303,"end":340},"obj":"Protein"},{"id":"T42","span":{"begin":1259,"end":1264},"obj":"Protein"},{"id":"T41","span":{"begin":1092,"end":1097},"obj":"Protein"},{"id":"T40","span":{"begin":1053,"end":1058},"obj":"Protein"},{"id":"T39","span":{"begin":972,"end":977},"obj":"Protein"},{"id":"T38","span":{"begin":930,"end":935},"obj":"Protein"},{"id":"T37","span":{"begin":919,"end":924},"obj":"Protein"},{"id":"T36","span":{"begin":912,"end":917},"obj":"Protein"},{"id":"T35","span":{"begin":488,"end":493},"obj":"Protein"},{"id":"T34","span":{"begin":342,"end":347},"obj":"Protein"},{"id":"T33","span":{"begin":303,"end":340},"obj":"Protein"},{"id":"T56","span":{"begin":1259,"end":1264},"obj":"Protein"},{"id":"T55","span":{"begin":1171,"end":1182},"obj":"Binding"},{"id":"T54","span":{"begin":1092,"end":1097},"obj":"Protein"},{"id":"T53","span":{"begin":1076,"end":1086},"obj":"Gene_expression"},{"id":"T52","span":{"begin":1053,"end":1058},"obj":"Protein"},{"id":"T51","span":{"begin":972,"end":977},"obj":"Protein"},{"id":"T50","span":{"begin":930,"end":935},"obj":"Protein"},{"id":"T49","span":{"begin":919,"end":924},"obj":"Protein"},{"id":"T48","span":{"begin":912,"end":917},"obj":"Protein"},{"id":"T47","span":{"begin":535,"end":542},"obj":"Positive_regulation"},{"id":"T46","span":{"begin":488,"end":493},"obj":"Protein"}],"relations":[{"id":"R11","pred":"equivalentTo","subj":"T45","obj":"T44"},{"id":"R12","pred":"themeOf","subj":"T46","obj":"T47"},{"id":"R13","pred":"themeOf","subj":"T52","obj":"T55"},{"id":"R14","pred":"themeOf","subj":"T52","obj":"T53"},{"id":"R15","pred":"themeOf","subj":"T54","obj":"T55"}],"text":"Tuberculosis (TB) disease in HIV co-infected patients contributes to increased mortality by activating innate and adaptive immune signaling cascades that stimulate HIV-1 replication, leading to an increase in viral load. Here, we demonstrate that silencing of the expression of the transcription factor nuclear factor of activated T cells 5 (NFAT5) by RNA interference (RNAi) inhibits Mycobacterium tuberculosis (MTb)-stimulated HIV-1 replication in co-infected macrophages. We show that NFAT5 gene and protein expression are strongly induced by MTb, which is a Toll-like receptor (TLR) ligand, and that an intact NFAT5 binding site in the viral promoter of R5-tropic HIV-1 subtype B and subtype C molecular clones is required for efficent induction of HIV-1 replication by MTb. Furthermore, silencing by RNAi of key components of the TLR pathway in human monocytes, including the downstream signaling molecules MyD88, IRAK1, and TRAF6, significantly inhibits MTb-induced NFAT5 gene expression. Thus, the innate immune response to MTb infection induces NFAT5 gene and protein expression, and NFAT5 plays a crucial role in MTb regulation of HIV-1 replication via a direct interaction with the viral promoter. These findings also demonstrate a general role for NFAT5 in TLR- and MTb-mediated control of gene expression."}